Recent research published in Nature reveals groundbreaking findings on IL-11, a protein whose inhibition can significantly extend the healthy lifespan of mice by nearly 25%. Conducted by scientists at the Medical Research Council Laboratory of Medical Science, Imperial College London, and Duke-NUS Medical School, the study demonstrated that deleting the gene responsible for producing IL-11 extended mouse lifespan by over 20%.
Key Findings in IL-11 Antibody Research
IL-11, a pro-inflammatory cytokine from the IL-6 family, is upregulated with age and negatively impacts healthspan and lifespan by activating the ERK–AMPK–mTORC1 axis.Mice with deleted Il11 or Il11ra1 genes showed protection against metabolic decline, multimorbidity, and frailty, resulting in a lifespan extension of approximately 24.9%.Administering anti-IL-11 antibodies to older mice improved metabolism, muscle function, reduced aging biomarkers and frailty, and extended lifespan by 22.5% in males and 25% in females.IL-11 regulates key signaling pathways involved in aging, including ERK, AMPK, mTOR, and JAK–STAT3. Inhibition of IL-11 leads to reduced activation of these pathways, mitigating the effects of aging.
The IL-11–ERK–mTORC1 signalling module is upregulated in ageing and associated with senescence and metabolic decline
Physiological Effects of IL-11 Inhibition
Old mice with inhibited IL-11 signaling exhibited improved glucose metabolism, lower body weight, reduced fat mass, and preserved lean mass. They also showed better glucose tolerance and insulin sensitivity.IL-11 is linked to cellular senescence, marked by increased levels of p16 and p21. Its inhibition reduces markers of senescence and inflammation in aged tissues.Inhibition of IL-11 reduces tissue fibrosis and improves mitochondrial function, preserving telomere length and mitochondrial DNA copy number.
Lifespan Extension with IL-11 Antibody Therapy
Mice with genetic deletion of Il11 or treated with anti-IL-11 antibodies showed significant lifespan extension, with reduced incidence of age-related cancers.Anti-IL-11 therapy is currently in early-stage clinical trials for fibrotic lung disease, suggesting potential translational opportunities for treating aging-related pathologies in humans.
Clinical Relevance and Potential Applications
Developing anti-IL-11 therapies for age-related diseases and conditions, potentially extending their use beyond fibrotic diseases to general aging interventions.Using IL-11 and its signaling pathways as biomarkers for aging and related pathologies, aiding in the early detection and monitoring of treatment efficacy.Further clinical trials are needed to test the efficacy and safety of anti-IL-11 therapies in extending human healthspan and lifespan, translating findings from mouse models to human applications.
Conclusion: IL-11 as a Target for Anti-Aging Therapies
This research underscores IL-11’s crucial role in promoting age-associated pathologies through its regulation of key signaling pathways involved in inflammation, metabolism, and cellular senescence. By inhibiting IL-11 signaling, either genetically or pharmacologically, significant improvements in healthspan and lifespan in mice were observed. This positions IL-11 as a potential therapeutic target for aging and age-related diseases.
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More information: Stuart Cook, Inhibition of IL-11 signalling extends mammalian healthspan and lifespan,Nature(2024).DOI:10.1038/s41586-024-07701-9. www.nature.com/articles/s41586-024-07701-9
Journal information: Nature
